About: IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury

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About: IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury
Creator	Abdipour, Amir Baylink, David Bi, Hongzheng Carreon, Edmundo Lyu, Justin Sutjiadi, Brian Tang, Xiaolei Wasnik, Samiksha Wilson, Sean Zhang, Jintao
Source	Medline; PMC
abstract	This study was undertaken to test two therapies for acute kidney injury (AKI) prevention, IGF-1, which is renal protective, and BTP-2, which is a calcium entry (SOCE) inhibitor. We utilized lipopolysaccharide (LPS) IP, as a systemic model of AKI and studied in five groups of animals. Three experiments showed that at 7 days: (1) LPS significantly reduced serum IGF-1 and intramuscular IGF-I in vivo gene therapy rescued this deficiency. (2) Next, at the 7-day time point, our combination therapy, compared to the untreated group, caused a significant increase in survival, which was noteworthy because all of the untreated animals died in 72 h. (3) The four pathways associated with inflammation, including (A) increase in cytosolic calcium, (B) elaboration of proinflammatory cytokines, (C) impairment of vascular integrity, and (D) cell injury, were adversely affected in renal tissue by LPS, using a sublethal dose of LPS. The expression of several genes was measured in each of the above pathways. The combined therapy of IGF-1 and BTP-2 caused a favorable gene expression response in all four pathways. Our current study was an AKI study, but these pathways are also involved in other types of severe inflammation, including sepsis, acute respiratory distress syndrome, and probably severe coronavirus infection.
has issue date	2020-06-08(xsd:dateTime)
bibo:doi	10.3390/ijms21114095
bibo:pmid	32521790
has license	cc-by
sha1sum (hex)	007b274b30fe62599356147bb29a960d30b17ee7
schema:url	https://doi.org/10.3390/ijms21114095
resource representing a document's title	IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury
has PubMed Central identifier	PMC7312627
has PubMed identifier	32521790
schema:publication	Int J Mol Sci
resource representing a document's body	covid:007b274b30fe62599356147bb29a960d30b17ee7#body_text
is schema:about of	named entity 'Our' named entity 'therapies' named entity 'Blockade' named entity 'TIME POINT' named entity 'EXPERIMENTS' named entity 'INTEGRITY' named entity 'RENAL' named entity 'INFLAMMATION' named entity 'SEVERE INFLAMMATION' named entity 'SOCE' named entity 'elaboration' named entity 'severe' named entity 'time point' named entity 'sublethal' named entity 'severe' named entity 'tissue' named entity 'calcium' named entity 'LPS' named entity 'NGAL' named entity 'kidney' named entity 'IGF-1' named entity 'LPS' named entity 'gene therapy' named entity 'calcium influx' named entity 'plasma membrane' named entity 'cytokines' named entity 'log-rank test' named entity 'homogenizer' named entity 'gene therapy' named entity 'plasma membrane' named entity 'IGF-1' named entity 'AKI' named entity 'AKI' named entity 'Streptavidin' named entity 'kidney' named entity 'calcium influx' named entity 'kidney' named entity 'cytosol' named entity 'transcription factor' named entity 'significant difference' named entity 'ng/mL' named entity 'IGF-1' named entity 'mice' named entity 'IGF-1' named entity 'morphology' named entity 'animal model' named entity 'cytosolic' named entity 'calcium transporter' named entity 'cytosolic' named entity '1-way ANOVA' named entity 'formalin solution' named entity 'mice' named entity 'LPS' named entity 'renal tubular function' named entity 'calcium influx' named entity 'Orai1' named entity 'periodic acid-Schiff' named entity 'calcium' named entity 'centrifuged' named entity 'IGF-1 deficiency' named entity 'combination therapy' named entity 'IGF-1' named entity '0.01' named entity 'LPS' named entity 'AKI' named entity 'AKI' named entity 'gene therapy' named entity 'LPS' named entity 'mice' named entity 'tail vein' named entity 'IL-1β' named entity 'therapeutic agents'

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